Removal of the facilitating effect of angiotensin II on sympathetic cardiovascular influences may enhance the antihypertensive effect of angiotensin converting enzyme (ACE) inhibitors but may also disturb reflexes involved in blood pressure homeostasis. To test this hypothesis in essential hypertensive subjects, the forearm vasomotor response to cardiopulmonary receptor deactivation (lower body negative pressure) was studied before and after acute or prolonged administration of captopril at doses capable of lowering blood pressure and blocking the formation of angiotensin II. After either acute or prolonged captopril administration there was less response (i.e. forearm vasoconstriction) than in the no-drug state. However, in the same subjects, another reflex response to cardiopulmonary receptor deactivation, the increase in plasma renin activity, was not blunted by the drug. Furthermore, the other major reflex responsible for blood pressure homeostasis, the arterial baroreflex, was left unchanged or was even favoured by administration of clinically effective doses of captopril. This finding applied to both the heart rate and the blood pressure modulating ability of the reflex (vasoactive drug and neck chamber techniques, respectively). Thus, reflex control of circulation may be adversely affected by ACE inhibition. However, this does not include all reflex targets and at least one major reflex is preserved following this pharmacological intervention. This may explain why our patients showed no orthostatic hypotension during chronic treatment with ACE inhibitors.

Mancia, G., Giannattasio, C., Grassi, G., Morganti, A., Zanchetti, A. (1988). Reflex control of circulation and angiotensin converting enzyme inhibition in man. JOURNAL OF HYPERTENSION SUPPLEMENT, 6(3), S45-S49.

Reflex control of circulation and angiotensin converting enzyme inhibition in man

MANCIA, GIUSEPPE
Primo
;
GIANNATTASIO, CRISTINA
Secondo
;
GRASSI, GUIDO;
1988

Abstract

Removal of the facilitating effect of angiotensin II on sympathetic cardiovascular influences may enhance the antihypertensive effect of angiotensin converting enzyme (ACE) inhibitors but may also disturb reflexes involved in blood pressure homeostasis. To test this hypothesis in essential hypertensive subjects, the forearm vasomotor response to cardiopulmonary receptor deactivation (lower body negative pressure) was studied before and after acute or prolonged administration of captopril at doses capable of lowering blood pressure and blocking the formation of angiotensin II. After either acute or prolonged captopril administration there was less response (i.e. forearm vasoconstriction) than in the no-drug state. However, in the same subjects, another reflex response to cardiopulmonary receptor deactivation, the increase in plasma renin activity, was not blunted by the drug. Furthermore, the other major reflex responsible for blood pressure homeostasis, the arterial baroreflex, was left unchanged or was even favoured by administration of clinically effective doses of captopril. This finding applied to both the heart rate and the blood pressure modulating ability of the reflex (vasoactive drug and neck chamber techniques, respectively). Thus, reflex control of circulation may be adversely affected by ACE inhibition. However, this does not include all reflex targets and at least one major reflex is preserved following this pharmacological intervention. This may explain why our patients showed no orthostatic hypotension during chronic treatment with ACE inhibitors.
Articolo in rivista - Articolo scientifico
Blood Pressure; Captopril; Carotid Sinus; Central Venous Pressure; Forearm; Heart; Humans; Hypertension; Lower Body Negative Pressure; Lung; Norepinephrine; Pressoreceptors; Reflex; Regional Blood Flow; Renin-Angiotensin System; Vascular Resistance
English
1988
6
3
S45
S49
none
Mancia, G., Giannattasio, C., Grassi, G., Morganti, A., Zanchetti, A. (1988). Reflex control of circulation and angiotensin converting enzyme inhibition in man. JOURNAL OF HYPERTENSION SUPPLEMENT, 6(3), S45-S49.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/59782
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